Drug-induced liver injury and anti-hepatotoxic effect of herbal compounds: a metabolic mechanism perspective

医学 肝损伤 药理学 药品 机制(生物学) 传统医学 认识论 哲学
作者
Jyoti Rani,Sanju Bala Dhull,Pawan Kumar Rose,Mohd. Kashif Kidwai
出处
期刊:Phytomedicine [Elsevier]
卷期号:122: 155142-155142 被引量:61
标识
DOI:10.1016/j.phymed.2023.155142
摘要

Drug-induced liver injury (DILI) is the most challenging and thought-provoking liver problem for hepatologists owing to unregulated medication usage in medical practices, nutritional supplements, and botanicals. Due to underreporting, analysis, and identification issues, clinically evaluated medication hepatotoxicity is prevalent yet hard to quantify. This review's primary objective is to thoroughly compare pharmaceutical drugs and herbal substances that have undergone clinical trials, focusing on their metabolic mechanisms contributing to the onset of liver illnesses and their hepatoprotective effects. The data was gathered from several online sources, such as PubMed, Scopus, Google Scholar, and Web of Science, using appropriate keywords. : The prevalence of conventional and herbal medicine is rising. A comprehensive understanding of the metabolic mechanism is necessary to mitigate the hepatotoxicity induced by drugs and facilitate the incorporation or substitution of herbal medicine instead of pharmaceuticals. Moreover, pre-clinical pharmacological research has the potential to facilitate the development of natural products as therapeutic agents, displaying promising possibilities for their eventual clinical implementation. Acetaminophen, Isoniazid, Rifampicin, Diclofenac, and Pyrogallol have been identified as the most often reported synthetics drugs that produce hepatotoxicity by oxidative stress, inflammation, apoptosis, and fibrosis during the last several decades. Due to their ability to downregulate many factors (such as cytokines) and activate several enzyme/enzyme systems, herbal substances (such as Gingko biloba, Curcumin, Resveratrol, Silymarin) provide superior protection against harmful mechanisms which induce hepatotoxicity with fewer adverse effects than their synthetic counterparts.
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